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DPT 503 > Neural Communication > Flashcards

Neural Communication Flashcards

1
Q

what is a synapse?

A

where a neuron and postsynaptic cell communicate

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2
Q

what are the components of a synapse?

A

a presynaptic terminal, postsynaptic membrane, and a synaptic cleft b/w the 2

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3
Q

axodendritic synapse

A

pre=axon
post=dendrite

most common synapse found in the body

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4
Q

axosomatic synapse

A

pre=axon
post=soma

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5
Q

axoaxonic synapse

A

pre and post=axon

axon terminal can synapse on distal axon or extreme distal axon near the terminal

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6
Q

dendrodendritic synapse

A

pre and post=dendrite

dendrite of one neuron synapsing on the dendrite of another neuron

not very common-only localized in certain areas for the brain

may be bidirectional signaling

may occur in diseased state where axodendritic synapses are damaged

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7
Q

what are the 2 forms of synaptic transmission?

A

electrical and chemical synapses

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8
Q

electrical synapses

A

gap junctions enable rapid and synchronized activity of many neurons

pore connections allow AP though pre and post

beneficial in cardiac muscle and its neurons

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9
Q

chemical synapses

A

key feature: synaptic vesicles filled with NTs

complex=slower but more flexible

  1. AP reaches presynaptic terminal and vesicles are brought down to terminal membrane
  2. Ca2+ enters presynaptic terminal through voltage gated Ca2+ channels bc inside has become more positive
  3. Ca2+ binds to docking proteins (SNARE) and vesicles fuse to membrane
  4. exocytosis: NT released into cleft
  5. NT binds to receptors on postsynaptic membrane and opens ion channels (ligand gated)
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10
Q

what are the effects of Botox

A

snips proteins that make up SNARE complex=no ACh into the cleft=no muscle contraction

no exocytosis of ACh

muscle paralytic

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11
Q

what happens to a NT after it’s used?

A

NT have to be inactivated/removed from receptors

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12
Q

what are the 3 mechanisms to eliminate NTs?

A

reuptake, degradation, diffusion

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13
Q

how does reuptake get rid of used NTs?

A

the NT is taken up, repackaged, and recycled

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14
Q

how does degradation get rid of used NTs?

A

when a NT is unbound and just existing in the cleft, an enzyme comes and deactivates it

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15
Q

how does diffusion get rid of used NTs?

A

the NT just diffuses away after it has done its job

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16
Q

what is an excitatory postsynaptic potential?

A

when the ion channel opens, makes the inside more positive, and depolarizes

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17
Q

how does the sodium channel result in an EPSP?

A

there is more sodium outside the cell, so when the channel opens, sodium will flow in making the inside more positive causing a depolarization

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18
Q

what is an inhibitory postsynaptic potential?

A

when the ion channel opens, makes the inside more negative, and depolarizes/hyperpolarizes

inhibits APs

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19
Q

how does the chloride channel result in an IPSP?

A

there is more chloride outside the cell, so when the channel opens, chloride flows in making the inside more negative causing a depolarization/repolarization

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20
Q

summation of postsynaptic potentials

A

one excitatory potential=depolarization

2 excitatory potentials=larger depolarization

inhibitory potential=some hyperpolarization

excitatory and inhibitory potential=depolarization if depolarization amplitude is greater than the inhibitory amplitude

2 excitatory and inhibitory potentials=depolarization larger than 1 excitatory and inhibitory but smaller than just 2 excitatory

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21
Q

what is presynaptic facilitation

A

a neuron excites the presynaptic neuron increasing transmission resulting in a large depolarization (EPSP)

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22
Q

what is presynaptic inhibition?

A

a neuron inhibits the presynaptic neuron decreasing transmission resulting in a smaller depolarization or hyperpolarization (IPSP)

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23
Q

what is presynaptic facilitory modulation of NT release?

A

an excitatory neuron increases the amount of NT released from the presynaptic neuron

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24
Q

what is presynaptic inhibitory modulation of NT released?

A

action of an inhibitory neuron on an axon decreases the amount of NT released from the presynaptic neuron

not every receptor is occupied so the response is decreased

25
Q

what is a real world example of presynaptic modulation of NT released?

A

pain perception:

when you think about a cut more it hurts more bc more NT is released

when you think about a cut less, it hurts less bc less NT is released

26
Q

what are the modulations of receptors?

A

down regulation and upregulation

27
Q

what is downregulation?

A

internalization decreases the number of receptors

inactivation/desensitization decreases the number of active receptors

28
Q

what is upregulation?

A

when the number of receptors increase or the receptors become hypersensitive

29
Q

are upregulation and downregulation reversible?

A

yes!

30
Q

what are the 2 types of transmission speeds?

A

fast transmission and slow transmission

31
Q

what is another name for fast transmission?

A

ionotropic

32
Q

what is another name for slow transmission?

A

metabotropic

33
Q

what is fast (ionotropic) transmission?

A

ligand-gated channels

a NT binds to the receptors, channels open, and ions flow through the channels

34
Q

what is slow (metabotropic) transmission? what are the 2 types? what do they in

A

more steps involved makes it slower and more flexible

G-protein coupled receptors:
- a protein is embedded in the membrane
- NT binds to the receptor, conformational changes occur, G-protein is activated, subunits float somewhere else

volume transmission:
- extrasynaptic release
- neuronal communication at variable distances
- NT not released into the cleft
- no particular target tissue

35
Q

how long does fast (ionotropic) transmission occur?

A

a millisecond to a minute

36
Q

how long does slow (metabotropic) transmission occur?

A

100s of milliseconds to days

37
Q

cholinergic

A

ACh

38
Q

glutamatergic

A

glutamate

39
Q

GABAergic

A

GABA

40
Q

glycinergic

A

glycine

41
Q

(nor)adrenergic

A

norepinephrine/epinephrine

42
Q

dopaminergic

A

dopamine

43
Q

serotonergic

A

serotonin

44
Q

histaminergic

A

histamine

45
Q

how are neurons classified?

A

by the NT they produce, release, or respond to

46
Q

ACh

A

excitatory

nicotinic
- ionotropic
- NMJ and CNS
- Alzheimers

muscarinic
- metabotropic
- CNS and PNS
- parasympathetic

47
Q

glutamate

A

excitatory

ionotropic

development, learning, and memory formation

non-NMDA
- AMPA and Kainate receptors
- sodium in=depolarization

NMDA:
- glycine acts a agonist
- magnesium block moved by depolarization of non-NMDA, then sodium and calcium can move in and potassium out

48
Q

GABA

A

inhibitory

CNS

GABAa
- ionotropic
- ligand-gated Cl- channels open and allow Cl- in making the inside more negative leading to a hyperpolarization

GABAb
- metabotropic

pathology: seizure, involuntary contraction, anxiety (over excitation of the brain)

49
Q

glycine

A

Inhibitory

BS and SC

one of the most abundant inhibitory NTs

learning and memory

ligand-gated Cl- channels open allowing Cl- in making the inside more negative causing a hyperpolarization

involved in NMDA receptor activation

pathology: (not enough) involuntary contractions

50
Q

dopamine

A

excitatory or inhibitory

motor control, cognition, reward mechanism, motivation

metabotropic

all throughout brain

pathology: addiction, Parkinson’s disease, schizophrenia

51
Q

norepinephrine (NE)

A

inhibitory or excitatory

attention and arousal

sympathetic: increased HR, BP, resp rate, vasodilation, vasoconstriction

metabotropic

too much=panic disorder, PTSD

epinephrine closely resembles NE

52
Q

serotonin

A

inhibitory

ionotropic and metabotropic

sleep, arousal, cognition, motor function, mood, pain perception

pathology-depression (lack of serotonin)

53
Q

amines

A

redundancy

complicates treatment bc it’s hard to know which NT is contributing to symptoms the most

NE, serotonin, and dopamine

54
Q

opioid peptides

A

inhibitory

endorphins, enkephalin, dynorphin

inhibit pain perception

SC, hypothalamus, BS

55
Q

substance P

A

excitatory

released by injured tissue and stimulates nerve endings at site of injury

CNS:
- relays pain signal from SC to brain
- hypothalamus and cerebral cortex
- pathology-pain syndrome

one of the most common neuropeptides in the body

nociceptive neurons

volume transmission-metabotropic

56
Q

nitric oxide

A

excitatory

gasotransmitter

acts through diffusion so it doesn’t require a receptor or membrane

vasodilation

long-term potentiation

seizure disorder

57
Q

co-transmission

A

multiple neurons released at the same synapse or from the same neuron

increased stimulus strength

pain info

depolarization=release of glutamate and substance P

slow pain and fast pain

58
Q

what are NT agonists

A

bind to receptors and has the same effects of the normal NT

same affinity and effects

59
Q

what are NT antagonists

A

bind to receptors and impedes the effects

prevents release of NT

ACE inhibitor, NMDA blocker, Botox

DPT 503 (22 decks)

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